Role of iNOS on the renal alterations induced by experimental sepsis in animals chronically treated with ethanol.

  • Autor
  • Sousa, AH1
  • Co-autores
  • Awata, WMC1,2 , Tirapelli, CR1
  • Resumo
  • Introduction: Sepsis is defined as an organ dysfunction with a potential risk of death, caused by a host’s unregulated response to an infection. Chronic ethanol consumption is also associated with renal dysfunction. The mechanism of renal damage caused by sepsis and ethanol consumption is related to oxidative stress and the increased production of nitric oxide (NO) by iNOS enzyme. Thus, this study aimed to evaluate the impact of chronic ethanol consumption in renal damage induced by sepsis, and the participation of iNOS in these responses. Methods: Male C57BL/6J mice (6 to 8 weeks aged and 20 to 25 g of weight) were treated for 12 weeks with ethanol and sub-lethal sepsis was induced by CLP model. To investigate iNOS participation, L-NIL, a selective inhibitor of iNOS, was used. 48 hours after induction of sepsis, animals were killed. Blood and renal cortex were collected. Ethics committee protocol approval number: 17.1.169.22.4. Results: Both sepsis and chronic ethanol consumption increased serum creatinine levels (mg/dL), and this response was not altered by treatment with L-NIL (C:0.15±0.01, n=5; E:0.23±0.01*, n=5; S:0.22±0.02*, n=7; ES:0.26±0.04*, n=6; L-C:0.12±0.01, n=8; L-E:0.16±0.01*, n=5; L-S:0.22±0.02*, n=10; L-ES:0.24±0.01*, n=9). Chronic ethanol consumption and sepsis also augmented superoxide generation (URL/mg protein), and this response was partially prevented by L-NIL treatment (C:307±20, n=6; E:412±26*, n=6; S:497±38*, n=8; ES:702±54*, n=7; L-C:195±15, n=8; L-E:217±11, n=9; L-S:395±19*, n=9; L-ES:356±8*, n=10). Conclusion: Both chronic ethanol consumption and sepsis leads to renal damage trough oxidative stress. Treatment with L-NIL, despite partially reducing the reactive oxygen species (ROS) generation, did not revert the renal dysfunction.

  • Palavras-chave
  • iNOS; Sepsis; Ethanol
  • Modalidade
  • Comunicação oral
  • Área Temática
  • Estresse oxidativo
Voltar
  • Estresse oxidativo
  • Disfunção endotelial
  • Produtos naturais
  • Inflamação e doenças vasculares
  • Sinalização celular
  • Tecido adiposo perivascular
  • Sistema endócrino e doenças vasculares
  • Revisões, projetos, revisões sistemáticas e metanálises em biologia vascular
  • Educação em saúde e doenças vasculares
  • COVID-19 e complicações vasculares

Comissão Organizadora

José Wilson do Nascimento Corrêa
Simone Potje
Gabriel Tavares do Vale
Stêfany Cau
Roger Lyrio
Simone R Potje
Alice Valença Araújo
Ruth Cristina Albuquerque Santos
Lara Caroline Amaro
Ana Dária Cassoli da Silva
Pollyana Peixoto
Izabela Moreira Bonfim
Jocimar José Pitol
Sunamita Vaz Martins
Izabela Moreira Bonfim
Palloma Emanuelle Dornelas de Melo
Daniella Bonaventura
Tagana Rosa
Sarah Victory Santana Gomes
Priscila Cruz
André Lucas Borges
Jéssyca Aparecida Soares Giesen
Leticia Tinoco Gonçalves
Silvia Maria Luna Alves
NAYANA YARED BATISTA
Wellington Francisco Pereira da Silva
Natália Ferreira de Araújo
Leandro de Carvalho Gomes

Comissão Científica